the heart and its dysfunctions

8/8/2019 The HEART and its dysfunctions

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Anatomy of the Heart

Hollow muscular organ

Lies obliquely in chest, behind sternum in mediastinum

Varies in size, depending on persons size; usually the size of the persons f ist

Heart Wall

Epicardium outermost layer

Myocardium middle and thickest layer

Endocardium innermost layer that lines heart valve and chambers

Pericardium consist of f ibrous pericardium and serous pericardium

Heart Chambers

Right atrium Left Atrium

Right ventricle Left Ventricle

Heart Valves Atrioventricular valves

Tricuspid valve

Mitral valve (bicuspid valve)

Semilunar valves

Pulmonic valve

Aortic valve

Coronary Blood Supply

Right coronary artery

Left main coronary artery (LAD, left circumflex)

About 75% of total coronary venous blood flow leaves left ventricle by way of coronarysinus.

Cardiac cycle

Includes the cardiac events that occur from the beginning of one heart beat to the

beginning of the next

Ventricular diastole (relaxation)

Ventricular systole(contraction)

Cardiac Output

Amount of blood the left ventricle pumps into the aorta per minute

Measured by multiplying heart rate times stroke volume

Cardiac output is 4-8 L per minute

3 Factors that Determine Stroke Volume

Preload degree of stretch on muscle f ibers when they begin to contract



Afterload amount of pressure left ventricle must work against to eject blood during

systole

Myocardial contractility ventricles ability to contract

Autonomic Innervation of the Heart

Sympathetic nerve stimulation causes release of norepeniphrine, which increases heart rate and

accelerates AV node conduction

Parasympathetic nerve stimulation causes release of acetylcholine, which slows heart rate and

conduction through AV node

Transmission of Electrical Impulse

Four key cell characteristics

Automaticity

Cells ability to spontaneously initiate an electrical impulse

Excitability

Cells ability to respond to an electrical impulse Conductivity

Cells ability to transmit an electrical impulse from one cell to another

Contractility

Cells ability to contract

Depolarization and Repolarization Cycle

Phase 0: Rapid Depolarization

Sodium moves rapidly into cell

Calcium moves slowly into cell

Phase 1:

Early

Repolarization

Sodium channels close

Phase 2: Plateau Phase

Calcium continues t flow in

Potassium continues to flow out

Phase3: Rapid Repolarization

Calcium channels close

Potassium flows out rapidly

Active transport via the sodium-potassium pump begins restoring potassium to the

inside of the cell and sodium to the outside of the cell

Phase 4: Resting Phase

Cell membrane is impermeable to sodium

Potassium moves out of the cell



Electrical Conduction System of the Heart

Impulses travel from SA node through internodaltracts and Bachmanns bundle to AV node

From AV node, impulses travel trough Bundle of His, bundle branches, and to Purkin je f ibers

SA node generates impulses of 60-100beats/minute

AV node can f ire cat a rate of 40-60beats/minute

Purkin je f ibers can f ire at rate of 20-40beats/minute

ECG BASICS

Application of Electrodes

Choose site over soft tissues or close to the bone; not over bony prominences, thick

muscles or skin folds

Skin Preparation

Use rough patch on back of electrode , dry washcloth, or gauze pad to rub each site until

skin reddens

Clip areas of dense hair

For oily skin, clean each site with alcohol pad, letting it air dry

SINUS TACHYCARDIA

Sinus rhythm at a rate equal to or greater than 100bpm

Etiology

Situations of increased physiologic demand for oxygen that occur in association with

stress, exercise, pain f ever, anemia, hypoxia and shock

Hyperthyroidism, heart failure, myocardial infarction, pulmonary embolism, excessve

caff eine and medications

Treatment

Beta-blockers and calcium channel blockers

SINUS BRADYCARDIA

A sinus rhythm with a rate less than 60bpm

Etiology

Vagal stimulation, sleep

Hypothyroidism, hypothermia, electrolyte imbalance

Inf erior wall myocardial infarction

Sick sinus syndrome

Medications

Treatment

Atropine and epinephrine

Pacemakers may be required if drug therapy is ineff ective



ATRIAL PREMATURE COMPLEXES

Results from a premature, ectopic, supraventricular impulse that originates somewhere

in the atria outside of the SA node.

Etiology

Stress, caff eine, alcohol

Heart failure, myocardial ischemia, valvular diseases, coronary artery disease

Chronic lung disease, hyperthyroidism, inf ection Electrolyte abnormalities; use of medications

PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA

Has an atrial rate from 150-250beats/min

Etiology

Caff eine

Marijuana use

Electrolyte imbalance

Hypoxia

Physical or psychological stress

Signs and symptoms

Rapid apical and peripheral pulse rate Hypotension

syncope

ATRIAL FLUTTER

A supraventricular dysrhythmia characterized by the appearance of sawtooth-shaped

flutter waves at a rate between 250-400bpm.

Etiology

Hyperthyroidism

Valvular disease

Ischemic heart disease, acute myocardial infarction

Pericardial disease Acute pulmonary embolism



Pulmonary disease

Congenital heart disease

ATRIAL FIBRILLATION

A supravenmtricular dysrhythmia characterized by multiple ectopic atrial foci,

uncoordinated atrial contractions, and a classically irregular ventricular rate

Etiology

Heart failure, ischemic heart disease

Valvular heart disease

Cardiomyopathy, alcohol, pericardial disease

Congenital heart disease

Sick sinus syndrome

Hypertension

Hyperthyroidism Lung disease

VENTRICULAR PREMATURE COMPLEXES

A premature ectopic impulse that originates somewhere in the ventricles below the

Bundle of His.

Herald lethal ventricular arrhythmia

CARDIOVASCULAR DYSFUNCTION

2 MAJOR GROUPS

1. Congenital heart disease

= includes primarily anatomic aberration present at birth that result in abnormal

cardiac function.

2. Acquired Cardiac Disease

= ref ers to disease processes or abnormalities that occur after birth and can be

seen in the normal heart or in the presence of congenital heart def ects.

ASSESSMENT

Health History Finding

1. Family history of congenital heart disorders

2. Presence of murmurs and age at which f irst noted

3. Feeding problems, including fatigue or diaphoresis during f eeding and poor weight gain 4. Respiratory diff iculties, including tachypnea, dyspnea, shortness of breath, cyanosis and

frequent respiratory inf ections

5.Chronic fatigue or exercise intolerance

6. Contact with known teratogens such as rubella during pregnancy

PHYSICAL ASSESSMENT

1. Growth abnormalities

2. Cyanosis

3. Clubbing of f ingers and toes

4. Periorbital and peripheral edema

5. Diminished peripheral pulses

6. Thready pulse



7.Engorged neck veins

8.Abdominal distention, hepatomegaly, spleenomegaly

9. Tachycardia, bradycardia, tachypnea

10. Hypotension or unequal blood pressure in arm and legs

11. Murmurs, bruits, thrills

DIAGNOSTIC TEST

A. Cardiac Catheterization

Types:

1. Diagnostic Catheterization

2. Interventional Catheterization

3. Electrophysiology Studies

NURSING MANAGEMENT

Preprocedural Care

1. Accurate height and weight measurement

2. Obtain history of allergic reaction to iodine

3. Assess and mark pulses before the patient goes to the catheterization room 4. Baseline oxygen saturation using pulse oximetry

5. NPO for 4-6 hours or more before the procedure according to institutional guidelines

Postprocedural Care

1. Assess for pulses, especially below the catheterization site for equality and symmetry

2. Assess for the temperature and color of the aff ected extremity

3. Vital signs every 15 minutes

4. Assess the dressing

5. Assess for the fluid intake

6. Watch out for hypoglycemia

7. Keep on bed with aff ected extremity straight for 4-6 hours after venous catheterization and 6-8

hours after arterial catheterization8. Encourage to void

9. B. Chest radiograph

10. C. Electrocardiography

11. D. Transthoracic

12. * M-Mode

13. *Two-dimensional

14. E. Doppler

15. *Fetal

16. *Trans-esophageal

17. F. Angiography

18. G. Electrophysiology

H. Exercise Stress Test

CONGENITAL HEART DISEASE

Pre-natal Contributory Factors

1. Maternal rubella during pregnancy

2. Maternal alcoholism

3. Maternal age over 40 years

4. Maternal type 1 diabetes

Genetic Factor

1. Has a sibling with a heart def ect

2. Parent with CHD

3. Chromosomal aberration such as Down Syndrome

CLASSIFICATION OF CHD

A. Acyanotic

1. Increased Pulmonary Blood Flow

Atrial Septal Def ect

Ventricular Septal Def ect

Patent Ductus Arteriosus

Atrioventricular Canal Def ect

2. Obstruction to Blood Flow from the Ventricle

Coarctation of Aorta

Aortic Stenosis

Pulmonic Stenosis



B. Cyanotic

1.Decreased Pulmonary Blood Flow

Tetralogy of Fallot

Tricuspid Atresia

2. Mixed Blood Flow

Transposition of Great Arteries

Total Anomalous Pulmonary Venous Return

Truncus Arteriosus

Hypoplastic Left Heart Syndrome

ATRIAL SEPTAL DEFECT

3 Types:

1. Ostium Primum

2. Ostium Secundum

3. Sinus Venosus Def ect

Manif estation

Murmur

Medical Management: Dacron Patch

Ventricular Septal Defect

Complication

1. CHF

2. Bacterial Endocarditis

3. Pulmonary Vascular Obstructive Disease

Management:

Palliative; pulmonary artery banding

Complete Repair

Atrioventricular Canal Defect

Consist of a low atrial septal def ect that is continuous with a high ventricular septal def ect and

cleft of the mitral and tricuspid valves

Surgical Treatment:

Patch closure of the septal def ect and reconstruction of the AV valve tissue

(either repair of the mitral valve cleft or fashioning of the AV valve)

Complication:

1. Heart block

2. Mitral regurgitation

3. Pulmonary hypertension

4. Congestive heart failure

Patent Ductus Arteriosus

Failure of the f etal ductus ateriosus to close within the f irst weeks of lif e

Complication:

1. Congestive Heart failure

2. Bacterial Endocarditis

3. Pulmonary Vascular Disease

Management:

1. Administration of Indomethacin

2. Surgical division or ligation of the patent vessel via a left thoracotomy

Coarctation of Aorta Localized narrowing near the insertion of the ductus arteriosus, resulting in increased

pressure proximal to the def ects and decresed pressure distal to the obstruction

Manif estation

Bounding pulses in arms

Weak or absent f emoral pulses

Cool lower extremities with lower blood pressure

Dizziness, headache, fainting and epistaxis

Complication:

1. Rupture aorta

2.Aortic aneurysm

3. Stroke



4. Congestive heart failure

Management:

1. Resection of coarcted portion with end to end anastomosis of the aorta

2. Enlargement of the constricted section using a graft of prosthetic material or a

portion of the left subclavian artery.

Medical Management:

Captopril ACE inhibitor

Nursing Responsibility:

1. Monitor BP and pulse rate often

2. Give drug 1 hour before meals

3. Separate doses with antacids

4. If patient develops f ever, sore throat, leukopenia, hypotension or tachycardia

withhold dose and notify the prescriber.

5. Inform that light headedness may occur

6. Use in caution during hot weather

Propranolol- Beta blocker

Nursing Responsibility:

1. Monitor BP, ECG and heart rate and rhythm, especially when giving IV route 2. Give oral drug with meals

3. Before any surgical procedure, notify anesthesiologist that patient is taking propranolol

4. Do not stop the drug abruptly

Aortic Stenosis

Narrowing or stricture of the aortic valve, causing resistance to blood flow in the left

ventricle

Manif estation

Faint pulses

Hypotension

Tachycardia

Poor f eeding

Exercise intolerance

Chest

Dizziness

Murmur

Management:

1. Aortic valvotomy

2. Valve replacement

3. balloon angioplasty

Complication:

1. Aortic insuff iciency

2. Valvular regurgitation

3. Tearing of valve leaflets

4. Loss of pulse in catheterized limb

Pulmonic Stenosis

Management:

1. Transventricular valvotomy

2. Balloon angioplasty

TETRALOGY OF FALLOT The classic form includes 4 def ects:

Vetricular septal def ect

Pulmonic stenosis

Overriding aorta

Right ventricular hypertrophy

Clinical manif estation

Blue spells or tet spells

Clubbing of f ingers

Squatting

Poor growth



Complication

Emboli

Cerebrovascular disease

Brain abscess

Seizure and loss of consciousness

Sudden death

TRICUSPID ATRESIA

There is no communication between the right atrium to the right ventricle

Clinical Manif estation

Cyanosis

Tachycardia

Dyspnea

Clubbing of f ingers

Management

Infusion of Prostaglandin E1 Modif ied Fontan Procedure

Systemic venous return is directed to the lungs through surgical connections

between thr right atrium and the pulmonary artery

TRANSPOSITION OF GREAT ARTERIES

The pulmonary artery leaves the left ventricle, and the aorta exits from the right

ventricle

TOTAL ANOMALOUS PULMORY VENOUS CONNECTION

The pulmonary veins are abnormally connected to the systemic venous circuit via the

right atrium or various veins draining toward the right atrium such as the superior vena

cava

ACQUIRED HEART DISEASES

TRUNCUS ATRESIA

Failure of normal septation and division of the embryonic bulbar trunk into the

pulmonary artery and the aorta, resulting in a single vessel that overrides both

ventricles

CONGESTIVE HEART FAILURE

Inability of the heart to pump an adequate amount of blood to the systemic circulation

at normal f illing pressures to meet the metabolic demands of the body.

Right-sided failure

The right ventricle is unable to pump blood eff ectively into the pulmonary artery

Left-sided failure

The left ventricle is unable to pump blood into the systemic circulation

Clinical manifestation of CHF

y Impaired Myocardial Function

Tachycardia

Sweating

Decreased urine output Fatigue

Weakness

Restlessness

Anorexia

Pale, cool extremities

Weak peripheral pulses

Decreased blood pressure

Cardiomegaly

Gallop rhythm



Pulmonary Congestion

Tachypnea

Dyspnea

Retractions

Flaring nares

Exercise intolerance

Orthopnea

Cough, hoarseness

Cyanosis

Wheezing

Grunting

Systemic Venous Congestion

Weight gain

Hepatomegaly

Peripheral edema

Ascites

Neck vein distention

Therapeutic management

Improve cardiac functions

Administration of digitalis glycosides (digoxin)

ACE inhibitor results in decreased pulmonary and systemic vascular resistance,

decrease blood pressure, and a reduction in afterload

Remove accumulated fluid

Fluid restriction, sodium restriction

Administration of diuretics

Decrease cardiac demands

Limit physical activity

Preserving body temperature

Treating any inf ections

Reducing the effort of breathing

Improve tissue oxygenation and decrease oxygen consumption

Supplemental cool, humidif ied oxygen

ISCHEMIC HEART DISEASE

An imbalance between the supply and demand of the heart for oxygenated blood

Conditions that Aggravate Ischemia

Increase in cardiac energy demand

Lowered systemic blood pressure

4 Syndromes

1. Myocardial Infarction

2. Angina Pectoris

3. Chronic Ischemic heart disease

4. Sudden cardiac death

Epidemiology

1.Prevention achieved by modif ication of determinants

2. Therapeutic advances

3. Maintenance of normal blood glucose levels in diabetic patients

4. Postmenopausal estrogen replacement therapy 5. Lipid lowering and antioxidant therapy

6. Aspirin prophylaxis

Pathogenesis

1. Role of Fixed Coronary Obstruction

2. Role of Acute Plaque Change

3. Role of Coronary Thrombus

4. Role of Vasoconstriction



ANGINA PECTORIS

Paroxysmal and usually recurrent attacks of substernal or precordial chest discomfort caused by

transient myocardial ischemia that falls short of inducing the cellular necrosis that def ines

infarction.

1. Stable Angina

Caused by reduction of coronary perfusion to a critical level by chronic

stenosing coronary atherosclerosis

Usually relieved by rest or nitroglycerine

2. Prinzmetal Variant Angina

Episodic angina that occurs at rest due to coronary artery spasm

Responds promptly to vasodilators, such as nitroglycerine and calcium channel

blockers

3. Unstable or Crescendo Angina

A pattern of pain that occurs with progressively increasing frequency, often

occurs at rest, and of more prolonged duration

MYOCARDIAL INFARCTION Also known as heart attack

Transmural

Involves full or nearly full thickness of the ventricular wall in the distribution of a

single coronary artery

Subendocardial Infarct

Ischemic necrosis limited to the inner one third of the ventricular wall

Risk Factors

Hypertension

Cigarette smoking

Diabetes mellitus

Genetic hypercholesterolemia

Blacks and white are aff ected equally

Men are signif icantly are at greater risk than women

Pathogenesis

1. Coronary Arterial Occlusion

Severe coronary atherosclerosis, acute atheromatous plaque change,

superimposed platelet activation, thrombosis and vasospasm.

2. Response of the Myocardium

Consequences and Complications of Myocardial Infarction

1. Contractile dysfunction

Left ventricular failure with hypotension, pulmonary vascular

congestion, pulmonary edema

2. Arrhythmias

Sinus bradycardia or tachycardia, ventricular premature contractions or

ventricular tachycardia, ventricular f ibrillation, or asystole

3. Myocardial rupture

Results from the mechanical weakening that occurs in necrotic and

subsequently inflamed myocardium

4. Pericarditis

5. Right ventricular infarction

6. Infarct extension

7. Infarct expansion

8. Mural thrombus 9. Ventricular aneurysm

10. Progressive late heart failures

Nursing interventions:

Encourage assessment of food intake and eating patterns to help identify areas that can

be improved

Discuss therapeutic lif estyle changes, dietary recommendations, emphasizing the role of

the diet in heart disease

Encourage gradual but progressive dietary changes

Discourage use of high fat, low-carbohydrate, or other fad diets for weight loss

Encourage reasonable goals for weight



Discuss risk factors for CHD, stressing that changing or managing those factors that can

be modif ied reduces the clients overall risk for the disease

y Discuss the immediate benef its of smoking cessation

y Help the client identify specif ic sources of psychosocial and physical support for smoking

cessation, dietary, and lif estyle changes

y Discuss the benef its of regular exercise for cardiovascular health and weight loss

y Provide information and teaching about prescribed medication such as cholesterol-

lowering drugs.

y STATINS= assess for muscle pain and tenderness

report digoxin toxicity

do not use for pregnant

women

Nicotinic acid

Give oral preparation with meals and accompanied by a cold beverage to

minimize GI eff ects

Administer with caution to clients with active liver disease, peptic ulcer disease,

gout or type 2 diabetes Monitor blood glucose, uric acid levels and liver function test during treatment

HYPERTENSION

BLOOD PRESSURE

- pressure exerted by blood on walls of the

blood vessels

- determined by CO, PVR, viscosity of the

blood, and the amount of circulating

blood volume

FACTORS THAT LEADS TO HPN

1. S

NS

overstimulation2. Alteration in baroreceptors and chemoreceptors

3. Increase in hormone

4. Changes in kidney function

Primary HPN

- chronic elevation of blood pressure

Secondary HPN

- a sign of another problems such as

kidney abnormality tumor of adrenal

gland, or a congenital def ect of the aorta

Isolated Systolic HPN

- a systolic pressure of 160 mmHg or

greater and a diastolic pressure of

90mmHg or less

Signs and Symptoms of HPN

1. Often none

2. Increase BP, bloody nose, severe anxiety or

shortness of breath

Diagnosis of HPN

1. Previous diagnosis of HPN

2. Presence of signs and symptoms, history of kidney or heart disease and current use of medication, increase BP

Risk Factors

Non-modif iable

1. family history of hypertension

2. age plaque build-up among elderly

3. ethnicity African-American (respond to

diuretics), European-Americans

chemical imbalances (respond to be beta blockers), Japanese-Americans

high sodium content of the diet, stress and cigarette smoking)

Modif iable Risk Factors

1. Weight reduction



2. Meal Planning

- salt intake

- caff eine

- intake of potassium (orange, banana,

brocolli), magnesium (spinach, nuts,

seeds, whole grains), calcium (milk,

yogurt, spinach)

3. Alcohol consumption

4. Exercise control hypertension by reducing weight,

decreasing peripheral resistance, and decrease body fat

5. Smoking

Therapeutic and Intervention

1. Lif estyle modif ication

2. Drug Theraphy

a. Diuretics increase urine output by

inhibiting sodium and water reabsorp-

tion by the kidneyPatent teaching:

1. Antihypertensive therapy must usually be

continued for the rest of their lives.

2. care

Complications:

1. Coronary Artery Disease

2. Atherosclerosis

3. Myocardial Infarction

4. Heart Failure

5. S

troke 6. Kidney Damage

7. Eye Damage

8. . Blood pressure should be well controlled before any invasive procedure

9. 4. Antihypertensive medication should be resumed as soon as possible after the procedure

10. Hypertensive emergency:

- a severe type of hypertension characterized

by elevation in SBP greater than 180mmHg

and diastolic BP greater than 120

- patients who are untreated, fail to comply with

antihypertensive therapy, or stop their

medication abruptly

the heart and its dysfunctions

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